Search results for "Cell Cycle"

showing 10 items of 804 documents

Apoptotic death induced by the cyclophosphamide analogue mafosfamide in human lymphoblastoid cells: Contribution of DNA replication, transcription in…

2007

Cyclophosphamide is one of the most often used anticancer drugs. Although DNA interstrand cross-links are considered responsible for its cytotoxicity, the mechanism of initiation and execution of cell death is largely unknown. Using the cyclophosphamide analogue mafosfamide, which does not need metabolic activation, we show that mafosfamide induces apoptosis dose and time dependently in lymphoblastoid cells, with clearly more apoptosis in p53(wt) cells. We identified two upstream processes that initiate apoptosis, DNA replication blockage and transcriptional inhibition. In lymphoblastoid cells, wherein DNA replication can be switched off by tetracycline, proliferation is required for induci…

DNA ReplicationProgrammed cell deathTime FactorsTranscription GeneticDNA damageDrug ResistanceAntineoplastic AgentsApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesToxicologyCaspase-Dependent ApoptosisCell Linechemistry.chemical_compoundMafosfamideHumansCHEK1PhosphorylationCyclophosphamideCaspaseCell ProliferationPharmacologyDose-Response Relationship DrugbiologyTumor Suppressor ProteinsCell cycleDNA-Binding ProteinsCheckpoint Kinase 2chemistryApoptosisCaspasesCheckpoint Kinase 1Cancer researchbiology.proteinTumor Suppressor Protein p53Protein KinasesSignal TransductionToxicology and Applied Pharmacology
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Resveratrol, a chemopreventive agent, disrupts the cell cycle control of human SW480 colorectal tumor cells

2002

Resveratrol is a natural polyphenolic compound produced by a number of plants and found in high amount in peanuts, seeds, grapes or berries as source of human nutrition. Epidemiological studies strongly suggest that resveratrol may act as a cancer chemopreventive compound. The mechanism by which resveratrol inhibits cell proliferation was studied in human colorectal tumor SW480 cell line. The results show that resveratrol strongly inhibits cell proliferation at the micromolar range in a time- and dose-dependent manner. Resveratrol appears to block the cell cycle at the transition --> G2/M since inhibition of [(3)H]-thymidine incorporation is not observed, while there is an increase of the c…

DNA Replicationendocrine system diseasesCellCyclin AAdenocarcinomaCyclin BProtein Serine-Threonine KinasesResveratrolS Phasechemistry.chemical_compoundCDC2 Protein KinaseStilbenesCDC2-CDC28 KinasesTumor Cells CulturedGeneticsmedicineAnticarcinogenic AgentsHumansCyclin B1Phosphorylationskin and connective tissue diseasesCyclinCyclin-dependent kinase 1biologyKinaseCell growthorganic chemicalsCell CycleCyclin-Dependent Kinase 2Cyclin-dependent kinase 2food and beveragesGeneral MedicineCell cycleFlow CytometryCyclin-Dependent KinasesGrowth InhibitorsNeoplasm ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureBiochemistrychemistryResveratrolEnzyme Inductionbiology.proteinCancer researchColorectal NeoplasmsProtein Processing Post-TranslationalCell DivisionInternational Journal of Molecular Medicine
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Class 1 Histone Deacetylases and Ataxia-Telangiectasia Mutated Kinase Control the Survival of Murine Pancreatic Cancer Cells upon dNTP Depletion

2021

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with a dismal prognosis. Here, we show how an inhibition of de novo dNTP synthesis by the ribonucleotide reductase (RNR) inhibitor hydroxyurea and an inhibition of epigenetic modifiers of the histone deacetylase (HDAC) family affect short-term cultured primary murine PDAC cells. We used clinically relevant doses of hydroxyurea and the class 1 HDAC inhibitor entinostat. We analyzed the cells by flow cytometry and immunoblot. Regarding the induction of apoptosis and DNA replication stress, hydroxyurea and the novel RNR inhibitor COH29 are superior to the topoisomerase-1 inhibitor irinotecan which is used to treat PDAC. Ent…

DNA Replicationendocrine system diseasesDNA damagereplication stressQH301-705.5RNR Inhibitor COH29Antineoplastic AgentsCell Cycle ProteinsRNRAtaxia Telangiectasia Mutated ProteinsArticle03 medical and health scienceschemistry.chemical_compoundAtaxia TelangiectasiaMice0302 clinical medicineHDACAnimalscancerPDAC cellsRibonucleotide Reductase SubunitEnzyme InhibitorsBiology (General)030304 developmental biology0303 health sciencesbiologyChemistryEntinostatDNA replicationapoptosisGeneral Medicine3. Good healthPancreatic NeoplasmsHistoneRibonucleotide reductase030220 oncology & carcinogenesisATMbiology.proteinCancer researchDNA damageHistone deacetylaseCells
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Cisplatin-induced endoreduplication in CHO cells: DNA damage and inhibition of topoisomerase II.

2006

It has been proposed that polyploid cells that arise during a variety of pathological conditions and as a result of exposure to genotoxicants, typically in the liver, become aneuploid through genetic instability. Aneuploidy contributes to, or even drives, tumour development. We have assessed the capacity of the drug cisplatin, one of the most commonly used compounds for the treatment of malignancies, to induce endoreduplication, a particular type of polyploidy, in cultured Chinese hamster AA8 cells. Taking into account that any interference with DNA topoisomerase II (topo II) function leads to endoreduplication, we have found that treatment of the cells with this platinum compound results i…

DNA damageHealth Toxicology and MutagenesisAntineoplastic AgentsCHO CellsPolyploidychemistry.chemical_compoundCricetinaeGeneticsmedicineEndoreduplicationAnimalsHumansTopoisomerase II InhibitorsEnzyme InhibitorsMolecular BiologyCisplatinbiologySettore BIO/16 - Anatomia UmanaTopoisomeraseChinese hamster ovary cellNeoplasms Second PrimaryCell cycleAneugensAneuploidyMolecular biologychemistryTopoisomerase II cisplatinbiology.proteinCancer researchTopoisomerase-II InhibitorCisplatinDNAmedicine.drugDNA Damage
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The DNA topoisomerase II catalytic inhibitor merbarone is genotoxic and induces endoreduplication

2012

Abstract In the last years a number of reports have shown that the so-called topoisomerase II (topo II) catalytic inhibitors are able to induce DNA and chromosome damage, an unexpected result taking into account that they do not stabilize topo II-DNA cleavable complexes, a feature of topo II poisons such as etoposide and amsacrine. Merbarone inhibits the catalytic activity of topo II by blocking DNA cleavage by the enzyme. While it was first reported that merbarone does not induce genotoxic effects in mammalian cells, this has been challenged by reports showing that the topo II inhibitor induces efficiently chromosome and DNA damage, and the question as to a possible behavior as a topo II p…

DNA damageHealth Toxicology and MutagenesisTopoisomerase II; Catalytic inhibitor; Merbarone; DNA damage; Clastogens; EndoreduplicationCatalytic inhibitorCell Linechemistry.chemical_compoundCricetulusCricetinaeGeneticsmedicineEndoreduplicationAnimalsTopoisomerase II InhibitorsClastogenMolecular BiologyAmsacrineCell ProliferationbiologyDNA synthesisCell growthTopoisomeraseMerbaroneCell cycleEndoreduplicationThiobarbituratesMolecular biologyTopoisomerase IIchemistrybiology.proteinDNAmedicine.drugDNA Damage
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2α-Hydroxyalantolactone from Pulicaria undulata: activity against multidrug-resistant tumor cells and modes of action.

2020

Abstract Background Sesquiterpene lactones having α-methylene-γ-lactone moiety are promising natural metabolites showing various biological activity. One of the major metabolites isolated from Pulicaria undulata, 2α-hydroxyalantolactone (PU-1), has not been investigated in detail yet. Multidrug resistance (MDR) represents a major obstacle for cancer chemotherapy and the capability of novel natural products to overcoming MDR is of great interest. Purpose Exploring the molecular modes of action for potent natural product metabolites. Methods The resazurin reduction assay was employed to evaluate the cytotoxicity of PU-1 on sensitive and their corresponding drug-resistant cell lines (overexpre…

DNA damagePharmaceutical ScienceApoptosisPulicaria03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineCell Line TumorDrug DiscoveryHumansPI3K/AKT/mTOR pathway030304 developmental biologyPhosphoinositide-3 Kinase InhibitorsPharmacology0303 health sciencesLeukemiaCell growthChemistryCell cycleG2-M DNA damage checkpointMolecular biologyAntineoplastic Agents PhytogenicBlotGene expression profilingG2 Phase Cell Cycle CheckpointsGene Expression Regulation NeoplasticComplementary and alternative medicineApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisMolecular MedicineSesquiterpenesDNA DamagePhytomedicine : international journal of phytotherapy and phytopharmacology
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DNA damage-induced cell death: From specific DNA lesions to the DNA damage response and apoptosis

2011

DNA damaging agents are potent inducers of cell death triggered by apoptosis. Since these agents induce a plethora of different DNA lesions, it is firstly important to identify the specific lesions responsible for initiating apoptosis before the apoptotic executing pathways can be elucidated. Here, we describe specific DNA lesions that have been identified as apoptosis triggers, their repair and the signaling provoked by them. We discuss methylating agents such as temozolomide, ionizing radiation and cisplatin, all of them are important in cancer therapy. We show that the potentially lethal events for the cell are O(6)-methylguanine adducts that are converted by mismatch repair into DNA dou…

DNA re-replicationCancer ResearchGuanineDNA RepairDNA repairDNA damageSurvivinAntineoplastic AgentsApoptosisBiologyInhibitor of Apoptosis ProteinsDNA AdductsNeoplasmsRadiation IonizingmedicineAnimalsHumansPhosphorylationCisplatinCell DeathCell CycleNF-kappa BDNA replicationDNAG2-M DNA damage checkpointCell cycleOncologyCancer researchDNA mismatch repairProto-Oncogene Proteins c-aktDNA DamageSignal Transductionmedicine.drugCancer Letters
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Myosin VIIa, harmonin and cadherin 23, three Usher I gene products that cooperate to shape the sensory hair cell bundle

2002

Deaf-blindness in three distinct genetic forms of Usher type I syndrome (USH1) is caused by defects in myosin VIIa, harmonin and cadherin 23. Despite being critical for hearing, the functions of these proteins in the inner ear remain elusive. Here we show that harmonin, a PDZ domain-containing protein, and cadherin 23 are both present in the growing stereocilia and that they bind to each other. Moreover, we demonstrate that harmonin b is an F-actin-bundling protein, which is thus likely to anchor cadherin 23 to the stereocilia microfilaments, thereby identifying a novel anchorage mode of the cadherins to the actin cytoskeleton. Moreover, harmonin b interacts directly with myosin VIIa, and i…

DNA ComplementaryCadherin Related ProteinsCell Cycle Proteinsmacromolecular substancesMyosinsBiologyTransfectionMicrofilamentGeneral Biochemistry Genetics and Molecular BiologyCell LineMiceCDH23Two-Hybrid System TechniquesHair Cells Auditoryotorhinolaryngologic diseasesmedicineAnimalsHumansProtein IsoformsRats WistarMolecular BiologyActinAdaptor Proteins Signal TransducingGene LibraryGeneral Immunology and MicrobiologyCadherinGeneral NeuroscienceStereociliaDyneinsCell DifferentiationArticlesCadherinsActin cytoskeletonActinsProtein Structure TertiaryRatsCell biologyCytoskeletal ProteinsMicroscopy Electronmedicine.anatomical_structureMicroscopy FluorescenceMyosin VIIasense organsCarrier ProteinsTip linkPCDH15HeLa CellsProtein BindingThe EMBO Journal
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Cytotoxic Activity of Organotin(IV) Derivatives with Triazolopyrimidine Containing Exocyclic Oxygen Atoms

2020

In this study cytotoxicity of organotin(IV) compounds with 1,2,4-triazolo[1,5-a]pyrimidines, Me3Sn(5tpO) (1), n-Bu3Sn(5tpO) (2), Me3Sn(mtpO) (3), n-Bu3Sn(mtpO) (4), n-Bu3Sn(HtpO2) (5), Ph3Sn(HtpO2) (6) where 5HtpO = 4,5-dihydro-5-oxo-[1,2,4]triazolo-[1,5-a]pyrimidine, HmtpO = 4,7-dihydro-5-methyl-7-oxo-[1,2,4]triazolo-[1,5-a]pyrimidine, and H2tpO2 = 4,5,6,7-tetrahydro-5,7- dioxo-[1,2,4]triazolo-[1,5-a]-pyrimidine, was assessed on three different human tumor cell lines: HCT-116 (colorectal carcinoma), HepG2 (hepatocarcinoma) and MCF-7 (breast cancer). While 1 and 3 were inactive, compounds 2, 4, 5 and 6 inhibited the growth of the three tumor cell lines with IC50 values in the submicromolar …

DenticityCellPharmaceutical Science01 natural sciencesAnalytical Chemistrychemistry.chemical_compoundDrug DiscoveryOrganotin CompoundstriazolopyrimidineCytotoxicityMembrane Potential MitochondrialCytotoxinsapoptosisBiological activityHep G2 CellsG2 Phase Cell Cycle CheckpointsGene Expression Regulation Neoplasticmedicine.anatomical_structureChemistry (miscellaneous)Mitochondrial MembranesMCF-7 CellsMolecular MedicineCyclin-Dependent Kinase Inhibitor p21crystal structurein vitro anticancer activityPyrimidineCell SurvivalStereochemistryorganotin(iv)010402 general chemistryArticlelcsh:QD241-441Inhibitory Concentration 50Structure-Activity Relationshiplcsh:Organic chemistrymedicineHumansPhysical and Theoretical ChemistryMetallodrug010405 organic chemistryLigandOrganic ChemistryTriazolesHCT116 CellsapoptosiG1 Phase Cell Cycle Checkpoints0104 chemical sciencesPyrimidineschemistrymetallodrugsCell cultureApoptosisDrug DesignTumor Suppressor Protein p53Reactive Oxygen SpeciesMolecules
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Monitoring of the action of drugs in melanoma cells by dynamic laser speckle

2014

Abstract. This work presents the development of a protocol based on the dynamic laser speckle designed tomonitor the reaction of cancer cells of line MEL-RC08 to the application of the drug Colcemid in two differentconcentrations: 0.2 and 0.4 μg∕mL. The protocol was designed using the forward scattering approach with anHe-Ne laser of 632.8 nm illuminating the samples, a control, and two variations of Colcemid, being monitoredalong 8 h. The data were analyzed numerically in the time and in the frequency domain, and the results pre-sented the ability of the technique to monitor the action of the drug, particularly Colcemid (0.4 μg∕mL). © 2014Society of Photo-Optical Instrumentation Engineers …

Diagnostic ImagingCellular activityComputer scienceBiomedical Engineeringlaw.inventionBiomaterialschemistry.chemical_compoundSpeckle patternKey pointOpticslawCell Line TumorImage Processing Computer-AssistedmedicineHumansInstrumentation (computer programming)MelanomaAnalysis of VarianceColcemidbusiness.industryLasersMelanomaCell CycleDemecolcineLasermedicine.diseaseAntineoplastic Agents PhytogenicAtomic and Molecular Physics and OpticsElectronic Optical and Magnetic MaterialschemistryFrequency domainbusinessBiomedical engineeringJournal of Biomedical Optics
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